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Mouse (Murine) Factor VII ELISA Kit für Sandwich ELISA - ABIN425161
Wang, Braun, Zhang, Norström, Thorlacius: Monocytes regulate systemic coagulation and inflammation in abdominal sepsis. in American journal of physiology. Heart and circulatory physiology 2015
Human Factor VII ELISA Kit für Sandwich ELISA - ABIN417285
Teligui, Dalmayrac, Corbeau, Bouquet, Godon, Denommé, Binuani, Verron, Boer, Baufreton: Ex vivo simulation of cardiopulmonary bypass with human blood for hemocompatibility testing. in Perfusion 2016
Hepsin (zeige HPN ELISA Kits) plays a physiologically important role in factor VII (zeige TH ELISA Kits) activation and hemostasis in zebrafish.
study reports the full-length cDNA sequences of rhesus monkey FVII; deduced protein sequence of FVII indicates the functional domains; comparison of three-dimensional protein structure with human shows high conservation between them
FVIIa binding to EPCR (zeige PROCR ELISA Kits) leads to a barrier protective effect in vivo
FVIIa binding to EPCR (zeige PROCR ELISA Kits) on the endothelium facilitates the transport of FVIIa from circulation to extravascular tissues where TF resides
Murine FVIIa binds poorly to murine EPCR (zeige PROCR ELISA Kits).
Conclude that the fVII-targeted verteporfin photodynamic therapy that we report here is a novel and effective therapeutic with improved selectivity for the treatment of breast cancer.
The participation of Egr-1 (zeige EGR1 ELISA Kits) in FVIIa-mediated regulation of keratinocyte function was confirmed by use of Egr-1 (zeige EGR1 ELISA Kits)-deficient mice, wherein a significant delay in skin wound healing after injury was observed, relative to WT mice.
Recombinant FVIIa readily associates with the vascular endothelium and subsequently enters into extravascular spaces where it is likely to bind to tissue factor (zeige F3 ELISA Kits) and is retained for extended time periods.
Gene targeting of tissue factor (zeige F3 ELISA Kits), factor X, and factor VII (zeige TH ELISA Kits) in mice: their involvement in embryonic development
true circadian rhythms for FVII were found
Data suggest that long-term expression of murine activated factor VII (zeige TH ELISA Kits) is safe, but elevated levels cause premature mortality.
tissue factor (zeige F3 ELISA Kits)/Factor VIIa/PAR2 (zeige F2RL1 ELISA Kits) signaling mediates neutrophil activation and fetal death in antiphospholipid syndrome and that statins may be a good treatment for women with aPL (zeige FASL ELISA Kits)-induced pregnancy complications.
Data suggest that, for all coagulation proteins tested (prothrombin, factor X, activated factor VII, activated protein C), tighter binding to lipid bilayers (lower Kd) is observed as the proportion of anionic phospholipid increases. These studies were conducted in high-throughput screening using phospholipid bilayers in nanodiscs with multiplexed silicon photonic sensor (micro-ring resonator) array technology.
A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa (zeige F10 ELISA Kits) complex activates FVIII (zeige F8 ELISA Kits) apart from thrombin (zeige F2 ELISA Kits) feedback.
Data suggest activation of PAR2 (zeige F2RL1 ELISA Kits) via FVIIA/TF signaling activates PI3K (zeige PIK3CA ELISA Kits)/AKT (zeige AKT1 ELISA Kits) signaling, inactivates GSK3b (zeige GSK3b ELISA Kits) signaling, leads to accumulation of beta-catenin (zeige CTNNB1 ELISA Kits), and promotes tumor cell migration/invasion. (PAR2 (zeige F2RL1 ELISA Kits) = protease-activated receptor 2 (zeige F2RL1 ELISA Kits); FVIIA = coagulation factor VIIa; TF = tissue factor/thromboplastin (zeige F3 ELISA Kits); PI3K (zeige PIK3CA ELISA Kits) = phosphatidylinositol 3-kinase; AKT (zeige AKT1 ELISA Kits) = proto-oncogene (zeige RAB1A ELISA Kits) protein c (zeige PROC ELISA Kits)-akt (zeige AKT1 ELISA Kits); GSK3b (zeige GSK3b ELISA Kits) = glycogen synthase kinase 3 beta (zeige GSK3b ELISA Kits))
heterozygotes for FVII deficiency show rare bleeding manifestations which are also present in the unaffected family members with normal FVII levels. This indicates that Factor VII (zeige TH ELISA Kits) activity levels played no role in the occurrence of the bleeding symptoms. Furthermore, FVII levels of around 0.40 IU/dl are capable of assuring a normal hemostasis.
Family-based association study revealed that the G allele of Protein Z (zeige PROZ ELISA Kits) rs2273971, and haplotypes GA, CG, and CGA (zeige CGA ELISA Kits) of Protein Z (zeige PROZ ELISA Kits) and factor VII (zeige TH ELISA Kits) had a significant effect on cerebral hemorrhage susceptibility.
Circulating FVII, FVIIa and TFPI (zeige TFPI ELISA Kits) were significantly elevated in women with severe preeclampsia in the absence of comparable changes in plasma TF levels.
Our study findings suggest a link between FVII and AR in prostate cancer pathogenesis.
Large deletions play a minor but essential role in the mutational spectrum of the F7 and F10 (zeige F10 ELISA Kits) genes. Copy number analyses (e. g. MLPA) should be considered if sequencing cannot clarify the underlying reason of an observed coagulopathy. Of note, in cases of combined FVII/FX deficiency, a deletion of the two contiguous genes might be part of a larger chromosomal rearrangement.
Structure-Function Relationship of the Interaction between Tissue Factor (zeige F3 ELISA Kits) and Factor VIIa.
Data suggest that allosteric regulation of FVIIa activity by tissue factor/thromboplastin (zeige F3 ELISA Kits) binding appear to involve direct interaction with FVIIa active site, stabilizing segment 215-217, activating loop 3, and leading to enhanced FVIIa activity.
This gene encodes coagulation factor VII which is a vitamin K-dependent factor essential for hemostasis. This factor circulates in the blood in a zymogen form, and is converted to an active form by either factor IXa, factor Xa, factor XIIa, or thrombin by minor proteolysis. Upon activation of the factor VII, a heavy chain containing a catalytic domain and a light chain containing 2 EGF-like domains are generated, and two chains are held together by a disulfide bond. In the presence of factor III and calcium ions, the activated factor then further activates the coagulation cascade by converting factor IX to factor IXa and/or factor X to factor Xa. Defects in this gene can cause coagulopathy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
coagulation factor VII
, clotting factor
, serum prothrombin conversion accelerator
, FVII coagulation protein
, eptacog alfa